Ricardo E Dolmetsch

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. pmc Using iPSC-derived neurons to uncover cellular phenotypes associated with Timothy syndrome
    Sergiu P Paşca
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California, USA
    Nat Med 17:1657-62. 2011
  2. pmc TrpC3 regulates hypertrophy-associated gene expression without affecting myocyte beating or cell size
    Jacob S Brenner
    Program in Chemical and Systems Biology, Stanford University, Stanford, California, United States of America Department of Neurobiology, Stanford University, Stanford, California, United States of America
    PLoS ONE 2:e802. 2007
  3. pmc A promoter in the coding region of the calcium channel gene CACNA1C generates the transcription factor CCAT
    Natalia Gomez-Ospina
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 8:e60526. 2013
  4. pmc Using induced pluripotent stem cells to investigate cardiac phenotypes in Timothy syndrome
    Masayuki Yazawa
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California 94305, USA
    Nature 471:230-4. 2011
  5. pmc The human brain in a dish: the promise of iPSC-derived neurons
    Ricardo Dolmetsch
    Department of Neurobiology, Fairchild Research Building, Room D227, Stanford University, Stanford, CA 94305, USA
    Cell 145:831-4. 2011
  6. pmc Timothy syndrome is associated with activity-dependent dendritic retraction in rodent and human neurons
    Jocelyn F Krey
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California, USA
    Nat Neurosci 16:201-9. 2013
  7. pmc STIM1 and calmodulin interact with Orai1 to induce Ca2+-dependent inactivation of CRAC channels
    Franklin M Mullins
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 106:15495-500. 2009
  8. pmc Modeling Timothy syndrome with iPS cells
    Masayuki Yazawa
    Department of Neurobiology, Stanford University School of Medicine, Stanford, CA, USA
    J Cardiovasc Transl Res 6:1-9. 2013
  9. doi request reprint SHANK3 and IGF1 restore synaptic deficits in neurons from 22q13 deletion syndrome patients
    Aleksandr Shcheglovitov
    Department of Neurobiology, Stanford University, Stanford, California 94305, USA
    Nature 503:267-71. 2013
  10. pmc LRRK2 mutant iPSC-derived DA neurons demonstrate increased susceptibility to oxidative stress
    Ha Nam Nguyen
    Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, CA 94305, USA
    Cell Stem Cell 8:267-80. 2011

Research Grants

  1. Calcium Channel Signaling in Neurons
    Ricardo Dolmetsch; Fiscal Year: 2004
  2. Calcium Channel Signaling in Neurons
    Ricardo Dolmetsch; Fiscal Year: 2005
  3. Calcium Channel Signaling in Neurons
    Ricardo Dolmetsch; Fiscal Year: 2006
  4. Calcium Channel Signaling in Neurons
    Ricardo Dolmetsch; Fiscal Year: 2007
  5. Calcium Channel Signaling in Neurons
    Ricardo Dolmetsch; Fiscal Year: 2006

Collaborators

Detail Information

Publications20

  1. pmc Using iPSC-derived neurons to uncover cellular phenotypes associated with Timothy syndrome
    Sergiu P Paşca
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California, USA
    Nat Med 17:1657-62. 2011
    ..These findings provide strong evidence that Ca(v)1.2 regulates the differentiation of cortical neurons in humans and offer new insights into the causes of autism in individuals with Timothy syndrome...
  2. pmc TrpC3 regulates hypertrophy-associated gene expression without affecting myocyte beating or cell size
    Jacob S Brenner
    Program in Chemical and Systems Biology, Stanford University, Stanford, California, United States of America Department of Neurobiology, Stanford University, Stanford, California, United States of America
    PLoS ONE 2:e802. 2007
    ..Thus TrpC3 may represent an important therapeutic target for the treatment of cardiac hypertrophy and heart failure...
  3. pmc A promoter in the coding region of the calcium channel gene CACNA1C generates the transcription factor CCAT
    Natalia Gomez-Ospina
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 8:e60526. 2013
    ..This study provides new insights into the regulation of CACNA1C, and provides an example of how exonic promoters contribute to the complexity of mammalian genomes...
  4. pmc Using induced pluripotent stem cells to investigate cardiac phenotypes in Timothy syndrome
    Masayuki Yazawa
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California 94305, USA
    Nature 471:230-4. 2011
    ..This study provides new opportunities for studying the molecular and cellular mechanisms of cardiac arrhythmias in humans, and provides a robust assay for developing new drugs to treat these diseases...
  5. pmc The human brain in a dish: the promise of iPSC-derived neurons
    Ricardo Dolmetsch
    Department of Neurobiology, Fairchild Research Building, Room D227, Stanford University, Stanford, CA 94305, USA
    Cell 145:831-4. 2011
    ..Recent work begins to tap this potential and also highlights challenges that must be overcome to be fully realized...
  6. pmc Timothy syndrome is associated with activity-dependent dendritic retraction in rodent and human neurons
    Jocelyn F Krey
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California, USA
    Nat Neurosci 16:201-9. 2013
    ..These results suggest that Ca(V)1.2 can activate RhoA signaling independently of Ca(2+) and provide insights into the cellular basis of Timothy syndrome and other ASDs...
  7. pmc STIM1 and calmodulin interact with Orai1 to induce Ca2+-dependent inactivation of CRAC channels
    Franklin M Mullins
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 106:15495-500. 2009
    ..These studies identify novel structural elements of STIM1 and Orai1 that are required for CDI and support a model in which CaM acts in concert with STIM1 and the N terminus of Orai1 to evoke rapid CRAC channel inactivation...
  8. pmc Modeling Timothy syndrome with iPS cells
    Masayuki Yazawa
    Department of Neurobiology, Stanford University School of Medicine, Stanford, CA, USA
    J Cardiovasc Transl Res 6:1-9. 2013
    ..The use of a human cellular model of cardiac arrhythmias provides a useful new platform not only to study disease mechanisms but also to develop new therapies to treat cardiac arrhythmias...
  9. doi request reprint SHANK3 and IGF1 restore synaptic deficits in neurons from 22q13 deletion syndrome patients
    Aleksandr Shcheglovitov
    Department of Neurobiology, Stanford University, Stanford, California 94305, USA
    Nature 503:267-71. 2013
    ..Our findings provide direct evidence for a disruption in the ratio of cellular excitation and inhibition in PMDS neurons, and point to a molecular pathway that can be recruited to restore it...
  10. pmc LRRK2 mutant iPSC-derived DA neurons demonstrate increased susceptibility to oxidative stress
    Ha Nam Nguyen
    Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, CA 94305, USA
    Cell Stem Cell 8:267-80. 2011
    ..This enhanced stress sensitivity is consistent with existing understanding of early PD phenotypes and represents a potential therapeutic target...
  11. pmc MicroRNA-mediated conversion of human fibroblasts to neurons
    Andrew S Yoo
    Howard Hughes Medical Institute and Department of Developmental Biology, Stanford University, Stanford, California 94305, USA
    Nature 476:228-31. 2011
    ..These studies indicate that the genetic circuitry involving miR-9/9*-124 can have an instructive role in neural fate determination...
  12. pmc Apelin enhances directed cardiac differentiation of mouse and human embryonic stem cells
    I Ning E Wang
    Division of Cardiovascular Medicine, Department of Medicine, School of Medicine, Stanford University, Stanford, California, United States of America
    PLoS ONE 7:e38328. 2012
    ..In conclusion, we have demonstrated that the treatment of apelin enhanced cardiac differentiation of mouse and human ESCs and exhibited synergistic effects with mesodermal differentiation factors...
  13. ncbi request reprint Molecular mechanisms of autism: a possible role for Ca2+ signaling
    Jocelyn F Krey
    Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Curr Opin Neurobiol 17:112-9. 2007
    ..These recent advances suggest a set of signaling pathways that might have a role in generating these increasingly prevalent disorders...
  14. pmc PIKfyve regulates CaV1.2 degradation and prevents excitotoxic cell death
    Fuminori Tsuruta
    Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Cell Biol 187:279-94. 2009
    ..These experiments identify a novel mechanism by which neurons are protected from excitotoxicity and provide a possible explanation for neuronal death in diseases caused by mutations that affect PtdIns(3,5)P(2) regulation...
  15. ncbi request reprint Induction of protein-protein interactions in live cells using light
    Masayuki Yazawa
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California, USA
    Nat Biotechnol 27:941-5. 2009
    ..These studies set the stage for the development of light-regulated signaling molecules for controlling receptor activation, synapse formation and other signaling events in organisms...
  16. pmc STIM1 clusters and activates CRAC channels via direct binding of a cytosolic domain to Orai1
    Chan Young Park
    Department of Neurobiology, Stanford University School of Medicine, CA 94305, USA
    Cell 136:876-90. 2009
    ..These studies establish a molecular mechanism for store-operated Ca(2+) entry in which the direct binding of STIM1 to Orai1 drives the accumulation and the activation of CRAC channels at ER-PM junctions...
  17. pmc The tumor suppressor eIF3e mediates calcium-dependent internalization of the L-type calcium channel CaV1.2
    Eric M Green
    Department of Neurobiology, Stanford University, 299 Campus Drive, Fairchild Research Building D227, Stanford, CA 94305, USA
    Neuron 55:615-32. 2007
    ..These findings provide a mechanism for activity-dependent internalization and trafficking of CaV1.2 and provide a tantalizing link between Ca2+ homeostasis and a mammalian oncogene...
  18. pmc Patient-specific induced pluripotent stem cells as a model for familial dilated cardiomyopathy
    Ning Sun
    Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Sci Transl Med 4:130ra47. 2012
    ..Thus, iPSC-derived cardiomyocytes from DCM patients recapitulate to some extent the morphological and functional phenotypes of DCM and may serve as a useful platform for exploring disease mechanisms and for drug screening...
  19. pmc Using light to control signaling cascades in live neurons
    Anshul Rana
    Graduate Program in Biochemistry, Stanford University, Beckman Center B400, 279 Campus Drive, Stanford, CA 94305, USA
    Curr Opin Neurobiol 20:617-22. 2010
    ....
  20. ncbi request reprint Behavioral abnormalities and circuit defects in the basal ganglia of a mouse model of 16p11.2 deletion syndrome
    Thomas Portmann
    Department of Neurobiology, Stanford University, Stanford, CA 94305 5345, USA School of Medicine, Stanford University, Stanford, CA 94305 5345, USA
    Cell Rep 7:1077-92. 2014
    ..Our findings unveil a fundamental role of genes affected by the 16p11.2 deletion in establishing the basal ganglia circuitry and provide insights in the pathophysiology of autism...

Research Grants6

  1. Calcium Channel Signaling in Neurons
    Ricardo Dolmetsch; Fiscal Year: 2004
    ..The results of these experiments will provide critical insights into how voltage-gated channels activate the signaling pathways that regulate the structure and function of the nervous system. ..
  2. Calcium Channel Signaling in Neurons
    Ricardo Dolmetsch; Fiscal Year: 2005
    ..The results of these experiments will provide critical insights into how voltage-gated channels activate the signaling pathways that regulate the structure and function of the nervous system. ..
  3. Calcium Channel Signaling in Neurons
    Ricardo Dolmetsch; Fiscal Year: 2006
    ..The results of these experiments will provide critical insights into how voltage-gated channels activate the signaling pathways that regulate the structure and function of the nervous system. ..
  4. Calcium Channel Signaling in Neurons
    Ricardo Dolmetsch; Fiscal Year: 2007
    ..The results of these experiments will provide critical insights into how voltage-gated channels activate the signaling pathways that regulate the structure and function of the nervous system. ..
  5. Calcium Channel Signaling in Neurons
    Ricardo Dolmetsch; Fiscal Year: 2006
    ..The results of these experiments will provide critical insights into how voltage-gated channels activate the signaling pathways that regulate the structure and function of the nervous system. ..